Although human airways are known to dilate during exercise, the neural mechanisms causing this increase in airway caliber have not yet been defined. The first goal of the proposed experiments, therefore, is to characterize the bronchodilator responses arising from the two neural mechanisms likely to function during exercise. The two mechanisms are: a reflex arising from contracting limb muscle, and central command arising from the subthalamic locomotor region. The second goal of the proposed experiments is to develop an understanding about the central neural pathways and integrating mechanisms mediating exercise- induced bronchodilation. The integrating mechanism is proposed to occur in the caudal ventrolateral medulla. The final common pathway to the airways is proposed to be the vagus nerve, whose inhibition by the two mechanisms is likely to cause the bronchodilation occurring during exercise. The proposed experiments will be performed in unanesthetized decerebrate dogs. Measurements of tracheal tension and total lung resistance will be used to characterize the increases in airway caliber in response to activation of central command and the reflex arising from dynamically contracting skeletal muscle. Central command will be activated by both electrical and chemical (i.e., d1- homocysteic acid and picrotoxin) stimulation of the subthalamic locomotor region. The reflex will be activated using "Kao type" stimulation of the L7-S, ventral roots. The bronchodilator responses to the two maneuvers will be measured before and after electrical and chemical destruction of the caudal ventrolateral medulla. The effects of the reflex and central command on the discharge of cells with vagal preganglionic fibers projecting to the lungs will be determined. The proposed experiments will be one of the first to examine how the brain regulates airway caliber.